Establishment of Acquired Immune Deficiency Mouse Model, and Its Mycobacterium intracellulare Infection.

近年来报道了许多获得性免疫缺陷综合征（AIDS）患者经常发生细胞内分枝杆菌感染。但是他们两人的待遇都很不令人满意。我们建立了胞内支原体感染小鼠模型，并利用该模型进一步探讨了其感染的治疗方法。采用单克隆抗小鼠Thy1.2抗体对胞内支原体感染模型小鼠进行免疫缺陷模型的建立。但不满意的免疫抑制是挣来的。因此，我们决定首先研究分枝杆菌感染的炎症细胞动力学。全肺灌洗（TPL）恢复炎性细胞，单克隆抗thy1.2、Lyt-2（CD8）、L3T4（CD4）和Ia染色。流式细胞仪检测细胞表面抗原表达。在感染过程中进行Tpls。感染后不久，Thy1.2阳性和Lyt-2阳性淋巴细胞增多，而L3T4阳性淋巴细胞和Ia阳性巨噬细胞在感染后3周逐渐增多。感染后6周，Thy1.2阳性淋巴细胞和Ia阳性巨噬细胞达到平台期。相反，Lyt-2阳性和L3T4阳性淋巴细胞的表面抗原表达率呈上下变化，呈反向旋转过程，仿佛相互反馈控制。下一步，研究生物反应修饰剂（BRMs）的作用。重组白介素-2 (il -2)， Muramyl二肽衍生物；细胞内感染小鼠给予DJ-7041和环孢素A （CyA）。观察il -2处理小鼠感染后早期和DJ-7041处理小鼠感染后晚期Ia阳性巨噬细胞的增加。利用该模型，我们拟建立一种类似艾滋病伴胞内支原体感染的免疫缺陷小鼠模型。

Recently many patients with acquired immune deficiency syndrome (AIDS) were reported to have frequent Mycobacterium intracellulare infection. But the treatment of both of them were quite unsatisfactory. We have established the M.intracellulare infection mouse model, and by using it, have investigated about the treatment of its infection further. For the purpose of establish the immune deficiency model, nomoclonal anti-mouse Thy1.2 antibody was administered to the M.intracellulare infection model mice. but unsatisfied immune depression was earned. So we decided to investigate the inflammatory cell dynamics for the mycobacterial infection at first. Inflammatory cells were recovered by total pulmonary lavage (TPL) and stained with monoclonal anti-Thy1.2, Lyt-2(CD8), L3T4(CD4), and Ia. The cell surface antigen expression were measured by flow cytometrical cell analizer. Tpls were performed during the course of infection. Thy1.2 positive and Lyt-2 positive lymphocytes were increased soon after the infection, but the L3T4 positive lymphocytes and Ia positive macrophages were gradually increased three weeks after infection. Thy1.2 positive lymphocytes and Ia positive macrophages reached the plateau six weeks after infection. On the contraty, Lyt-2 positive and L3T4 positive lymphocytes were up and down with their surface antigen expression ratio and have a contra-rotation course as if they were feed back controlled each other. For the next step, the effects of biological response modifiers (BRMs) were investigated. Recombinant interleukin-2 (rIL-2), Muramyl dipeptide derivative; DJ-7041 and cyclosporin A (CyA) were administered to the M.intracellulare infection mice. The increase of Ia positive macrophages at the early stage after infection by rIL-2 treated mice and at the late stage by DJ-7041 treated mice were observed. By using this model we are going to establish the immune deficiency mouse model akin to the AIDS with M.intracellulare infection.